Genetic studies on the transmission of murine retroviruses through the mouse germline, susceptibility to exogenous infection, and virus-induced oncogenis have led to the identification and chromosomal mapping of numerous genetic loci involved in these phenomena. The analysis of somatic cell hybrids has been used either alone or in conjunction with classical Mendelian crosses to map the following genes: mouse mammary tumor proviral loci to chromosome 14 in C3H/HeJ mice and to chromosome 6 in BALB/c and an endogenous MuLV provirus to chromosome 11; the cellular homologs of 3 oncogenes to 3 chromosomes; tumor-specific ecotropic MuLV integration sites to chromosomes 7, 15 and 19; tumor-associated mammary virus integration sites to 3 different chromosomes; and the interferon Beta-1 genes to chromosome 4. Hybrid cells have also been used to analyze the differential expression of endogenous murine leukemia viral loci in chemically induced hybrid cells which lack the receptors required for secondary infection. The role of the ecotropic cell surface receptor has also been examined in target cell recognition by autoreactive thymocytes.